Background: The complexity of the glaucoma pathophysiology is directly reflected on its experimental modeling for studies about pathological mechanisms and treatment approaches. Currently, a variety of in vivo models are available for the study of glaucoma, although they do not reach an exact reproduction of all aspects characterizing the human glaucoma. Therefore, a comprehensive view of disease onset, progression and treatment efficacy can only be obtained by the integration of outcomes deriving from different experimental models.
Methods: The present article summary experimental procedures and analytical methodologies related with two experimental models of glaucoma belonging to the classes of induced intraocular pressure (IOP)-elevation and genetic models, methyl cellulose (MCE)-induced ocular hypertension and DBA/2J mouse strain. Point-by-point protocols are reported with a particular focus on the critical point for the realization of each model. Moreover, typical strength and drawbacks of each model are described in order to critically handle the outcomes deriving from each model.
Discussion: This paper provides a guideline for the realization, analysis and expected outcomes of two models allowing to study IOP-driven neurodegenerative mechanisms rather than IOP-independent neurodegeneration. The complementary information from these models could enhance the analysis of glaucomatous phenomena from different points of view potentiating the basic and translational study of glaucoma.
Background: Bacillary layer detachment (BALAD) is a phenomenon characterized by fluid accumulation at the myoid region of the inner photoreceptor segments identifiable on optical coherence tomography (OCT) imaging. This finding has been recently described in patients with diverse primary diagnoses which share the common feature of serous exudation in the posterior pole. However, thus far there have been very few reports in the literature of BALAD in patients with posterior scleritis.
Case Description: A 16-year-old male presented with unilateral vision changes that acutely worsened overnight to significant unilateral vision loss. He was eventually diagnosed with idiopathic posterior scleritis with associated BALAD on OCT. Similar to other reported cases of BALAD, he experienced anatomic restoration of the outer retina followed by good visual recovery after treatment with high dose steroid, ultimately with complete recovery of both retinal anatomy and vision within 4 months.
Conclusions: This case provides further evidence that posterior scleritis can be a cause of BALAD. The rapid presentation and excellent visual and anatomical outcome of this case is entirely consistent with known descriptions of BALAD in a variety of other conditions, further supporting the categorization of BALAD as an entity which retinal specialists should be able to recognize as distinct from other forms of intraretinal fluid, retinal detachment, and retinoschisis.
Background: The complexity of the glaucoma pathophysiology is directly reflected on its experimental modeling for studies about pathological mechanisms and treatment approaches. Currently, a variety of in vivo models are available for the study of glaucoma, although they do not reach an exact reproduction of all aspects characterizing the human glaucoma. Therefore, a comprehensive view of disease onset, progression and treatment efficacy can only be obtained by the integration of outcomes deriving from different experimental models.
Methods: The present article summary experimental procedures and analytical methodologies related with two experimental models of glaucoma belonging to the classes of induced intraocular pressure (IOP)-elevation and genetic models, methyl cellulose (MCE)-induced ocular hypertension and DBA/2J mouse strain. Point-by-point protocols are reported with a particular focus on the critical point for the realization of each model. Moreover, typical strength and drawbacks of each model are described in order to critically handle the outcomes deriving from each model.
Discussion: This paper provides a guideline for the realization, analysis and expected outcomes of two models allowing to study IOP-driven neurodegenerative mechanisms rather than IOP-independent neurodegeneration. The complementary information from these models could enhance the analysis of glaucomatous phenomena from different points of view potentiating the basic and translational study of glaucoma.
